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Elife. 2019 May 2;8. pii: e45051. doi: 10.7554/eLife.45051. [Epub ahead of print]

The long non-coding RNA Cerox1 is a post transcriptional regulator of mitochondrial complex I catalytic activity.

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MRC Human Genetics Unit, Institute of Genetics and Molecular Medicine, University of Edinburgh, Edinburgh, United Kingdom.
MRC Functional Genomics Unit, University of Oxford, Oxford, United Kingdom.
Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford, United Kingdom.
British Heart Foundation Centre for Cardiovascular Science, University of Edinburgh, Edinburgh, United Kingdom.
Department of Biochemistry, University of Oxford, Oxford, United Kingdom.


To generate energy efficiently, the cell is uniquely challenged to co-ordinate the abundance of electron transport chain protein subunits expressed from both nuclear and mitochondrial genomes. How an effective stoichiometry of this many constituent subunits is co-ordinated post-transcriptionally remains poorly understood. Here we show that Cerox1, an unusually abundant cytoplasmic long noncoding RNA (lncRNA), modulates the levels of mitochondrial complex I subunit transcripts in a manner that requires binding to microRNA-488-3p. Increased abundance of Cerox1 cooperatively elevates complex I subunit protein abundance and enzymatic activity, decreases reactive oxygen species production, and protects against the complex I inhibitor rotenone. Cerox1 function is conserved across placental mammals: human and mouse orthologues effectively modulate complex I enzymatic activity in mouse and human cells, respectively. Cerox1 is the first lncRNA demonstrated, to our knowledge, to regulate mitochondrial oxidative phosphorylation and, with miR-488-3p, represent novel targets for the modulation of complex I activity.


biochemistry; chemical biology; genetics; genomics; human; mouse

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Conflict of interest statement

TS, KR, WH, OB, SR, JT, NL, LH, RC, SC, AF, JW, NM, AM The other authors declare that no competing interests exist. CP Chris P Ponting, Reviewing editor, eLife.

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